Dopamine and serotonin are both a type of chemical known as a neurotransmitter. There are many different types of neurotransmitter, and many different types of each type. The brain is made up of long cells known as neurons, which pass electrical currents from one to the next. In between each neuron is an extremely small gap called a synapse. In order to send the signal from one neuron to the next, the electrical signal needs to jump this gap - but it can't. In order to do this, the neuron sending the signal releases neurotransmitters into the synapse, which float across and bind to the receiving neuron. This then effects the activity of the receiving neuron, either by increasing or decreasing its electrical activity.

If you are asking what is the function of serotonin or dopamine, it depends on where in the brain they are being released. Both chemicals are released in a wide variety of brain regions, and the effect of their release depends on the types of neurons and their wiring in those different regions.

Dopamine is quite often tagged as the 'reward' chemical, because it is released in the 'reward pathway'. It is not a coincidence that recreational drugs also bind to the same receptor sites as dopamine! But it has also been shown to be involved in arousal, motor control and even lactation.

The release of serotonin is thought to be often involved in apetite and mood. The widely used anti-depressent, Prozac, is a serotnin re-uptake inhibitor. When you take this drug, it slows down the rate that serotonin is re-absorbed after being released into the synapse. This means there is more serotonin floating around in the synapse, and so it is more likely to bind to, and effect the neurons involved in making us feel depressed.

Actually, most recreational drugs don't bind to the dopamine receptor itself. Cocaine and amphetamines work by modulating the dopamine re-uptake transporter. Antipsychotics, on the other hand, can act as direct agonists or antagonists to the dopamine receptor. Sorry for nitpicking :)

It's worth noting that most (selective) dopamine receptor agonists (i.e, Pramipexole, Cabergoline, Ropinirole) tend to have little to no recreational value. There's a few recreational drugs that bind to dopamine receptors directly, but it isn't their main action -- LSD for example.

Most antipsychotics tend to be very "dirty" receptor ligands. For most, the effects tend to mediated as much by serotonergic effects as dopaminergic effects.

I will assume that you are asking what these terms means in general. In order for anything interesting to happen in a biological system, some kind of messenger must bind to a receptor.

Receptors are fairly specific to their specific messengers. The classic way of teaching this is the lock and key model. You may have bumped into this if you ever studied enzymes in high school. A receptor is like a lock that needs a perfectly matching key in order to activate it. The messenger, which is usually very very small in compared to the receptor binds (temporarily chemically attaches) to an active site on the receptor.

However, unlike a lock and key, a receptor does need a perfect match. Imagine if the keyhole on your lock was made out of firm rubber. Anything "close enough" to your key would still probably work if you jammed it in hard enough. However, if you cram it in, not everything might line up properly, and the lock might not be able to open.

Similarly, a receptor's active zone does not need an exact match of its expected messenger. This is the basis of drug design. An agonist is something that binds to a receptor and activates its function. Like a key opening a lock. Receptors typically have endogenous agonists which are the chemicals that the body makes that are designed to target that receptor. We can also make drugs that target the receptor by being close enough to the endogenous agonist to still activate it, while still having some different properties.

An antagonist is like a key that doesn't quite fit. It will bind to the receptor just fine, but it will not activate the receptor's function. In doing so, it will however block other agonists from binding there by competing with them for binding sites. If an antagonist is bound to the receptor, an agonist cannot bind there. This also means that an antagonist has no effect unless the agonist is also present since all it does is compete with the agonist for binding sites.

Just a nit pick that a partial agonist will bind to the receptor and activate its function, but not as much as a complete agonist. In a competitive environment (where both the complete and partial agonists exist), the partial agonist may actually reduce the activity of the receptor by preventing the complete agonist from binding to the receptor and completely activating it.

Kind of. But there are various types of antagonists as well. Competitive antagonists fit your analogy closest. Irreversible antagonists are like throwing a bomb at a server. There are also inverse agonists, which bind to receptors and then elicit an effect opposite that of agonists (vs antagonists which prevent agonists from binding to the receptor).

And some antagonists also exhibit inverse agonist behavior. Competitively blocking regular agonists while also binding and eliciting some sort of response that is opposite to that of regular agonists.

I would just like to emphasize how complicated the brain is. We use SSRI's to treat depression because they work, not because Serotonin = happiness. My favorite example of this is how Selective Serotonin Reuptake ENHANCERS (look up Stablon) are also used to treat depression even though neurologically they work exactly opposite to SSRI's like Prozac.

For example, I've seen compelling logic arguing that dopamine may be directly related to feelings of motivation, rather than indirectly responsible through a reward pathway that simply makes the results of motivation feel good. Not being an expert in the field, though, I'm not sure how confident the consensus really is... though I get the distinct sense that neuroscience is generally not very confident about a great many things at this time.

Before one can make a general consensus that a specific biological molecule, like dopamine, can be related to a specific "feeling" or set of feelings, one must first understand the mechanism. That is something neuroscience has been fairly successful in investigating. However, there are probably more ways and places/receptors dopamine can act that we currently know.

Dopamine can bind to many receptors, including D1 and D2 receptors. D1 receptors are essentially upregulate activity in whatever post-synaptic neuron they are located on. D2 receptors can be seen ad down-regulating activity on the post-synaptic neuron they are on.

In short, the function/effect is less important than the class of receptor and binding site. Also important, as already stated, is the location and identityof the neuron being stimulated by dopamine. When taking location into account, one must consider both the origin and the destination. This gives us insight on the entire pathway. What sort of stimulus initiated the cascade? How is it encoded? What neurons/regions is this information communicating with? What will the end result/behavioral output be based on what we know of the origin, nature, and destination of the impulse?

Edit: also note that even though D1 receptors are seen as upregulating and D2 is considered to be down-regulating. The change in activity is only for that specific neuron. What I mean by that is, suppose you down regulate the activity of a neuron that is currently inhibiting another neuron. The net effect from this isolated example could be seen as positive or up-regulatory.

Electrical currents in the brain are caused by the imbalance of different ions across the cell membrane, resulting in a voltage difference from the inside of the cell to the outside of the cell. Neuroscientists think of current as the flow of protons, i.e. sodium (Na+) and potassium (K+) ions, although Chloride, calcium, and other charged particles do have contributions to the cells membrane potential. Currents are propagated via the opening and closing of specific ion channels that can be selective or non-selective for certain ion species. So basically, the electrical currents in the brain are made from the very complex and highly coordinated process of ion channels opening and closing.

The statement that electrical currents can't pass between neurons without transmitters is false. In the old days, there were 2 schools of thought on how signaling work. Was it electrical or chemical? Well it turns out it is both. Electrical signaling between 2 neurons or other brain cell types (glia) can occur through gap junctions, which are basically pores that link the cells together and allows current to flow directly through one cell to the next. Gap junction transmission is therefore faster and is used in nature to mediate many fast, reflexive responses, such as the crayfish escape reflex. We also have these types of connections in our brains.

Signals can also be passed on chemically via neurotransmitters. The important thing to know here is that the neurotransmitter itself isn't directly responsible for change in electrical current. When a neurotransmitter binds to a receptor, the receptor itself is often an ion channel (or it can be a signaling receptor that has downstream effects that lead to ion channels opening/closing). So when a neurotransmitter (or drug) binds to a receptor, the receptor will undergo a conformational change that leads to channel opening and ions flowing in/out. Depending on the type of channel, the signal can be excitatory (i.e. it raises the membrane potential) or inhibitory (i.e it lowers the membrane potential). So a neurotransmitter like Acetylcholine or a drug like nicotine binds to its receptor and opens a sodium channel that lets sodium ions flow into the cell and the cell's membrane potential will be depolarized, leading to downstream changes that allow the signal to be propagated. On the other hand, a signal can be inhibitory because the transmitter that binds opens a chloride channel that lows the membrane potential and causes the signal to halt from propagating.

You could probably ask a million more questions based on this and it's obviously more complex than what I've described but that's the basic gist

There is an actual physical gap between the two cells (neurons). Electrical signals in neurons are generated due to the difference in charge between the inside and outside of the cell. This is the cell voltage.

When a neuron sends a signal it is initiated from an influx of ions which changes the cell voltage. This is referred to as an action potential and it travels the length of the cell. Once it reaches the end, it cant just magically pass on its charge to the neighboring cell, b/c they are not physically connected. This is where the neurotransmitters (NTs) come into play. When the action potential reaches the synapse (place where 2 neurons meet) it signals NTs to be released from the pre-synaptic neuron (the one carrying the action potential). The NTs "float" across the gap and activate receptors on the post-synaptic neuron. Those receptors then can go on to produce another action potential, or a variety of other things as doofangoodle mentioned above

To visualize what Rubixx_Cubed is describing, this is a basic image of a neuron. The dendrites of one neuron connects with the axon terminals (synapses) of another. When the neurotransmitter is released from one neuron, it connects on the dendrites of the next neuron. That's how the process begins and continues to the next cell.

SSRIs bind to serotonin transporters to block their action on the reuptake of serotonin into the neuron, resulting in an increase of serotonin in the synapse, whereas MDMA binds to serotonin transporters (and vesicular monoamine transporters) to reverse their action and release serotonin from inside the cell into the synapse. It's pretty much the opposite in terms of action, but the result is a net increase in extracellular serotonin in both cases.

MDMA is an inhibitor of serotonin storage, and it binds to serotonin receptors. Generally amphetamines interfere with a cell's ability to store neurotransmitters like serotonin, causing an increase in the amount of serotonin, since it can't be transported out. The amphetamines take the place of the serotonin.

Prozac is a selective serotonin reuptake inhibitor. What that means is that Prozac blocks the serotonin reuptake transporters.

They seems really close, so if someone better than me can help, that would be awesome. But it seems like the difference is that MDMA occupies the serotonin transporters, so there is an increase of serotonin. And Prozac occupies the space the serotonin transporters should be, in the first place, so the serotonin has no way to leave. MDMA rides shotgun in the car so you can't get to where you want to go. Prozac just takes your parking space. Eh?

Would it be possible for you to expand on what exactly the reward pathway is? I understand how it can be increased or inhibited through dopamine and serotonin, but do we understand what actually causes the effects of happiness?

The reward pathway is, in its simplest form, the connections from the area of the brain called the ventral tegmental area to another area called the nucleus accumbens. During a rewarding experience, dopamine is released from neurons originating in the VTA onto neurons in the nucleus accumbens, resulting in pleasurable sensations. What is actually causing us to experience the sensation? Not too sure..

Just be forewarned, don't get too attached to a notion of neurotransmitters having a thematic or dominating function. Nature uses them all over the place, often implementing them in weird spots. The only real constant (kind of) is the effect of a specific neurotrasmitter-receptor pair within a neuron's internal events.

There are lots of neurotransmitters, and synapses that use dopamine and serotonin are actually pretty rare in the brain. This is compounded by the fact that there is a wide variety of receptor proteins for each neurotransmitter. The same neurotransmitter binding to different receptors can result in different things. For instance, LSD binds to and activates only one type of seotonin receptor. The two most common neurotransmitters by far are glutamate and GABA. The reason neurotransmitters like dopamine and serotonin are more well known is because many drugs act on their synapses, and whereas drugs that act on GABA and glutamate are poisons. To finish without rambling anymore, there is a huge variety of neurotransmitters with different properties and effects, many of which are poorly understood.

For instance, LSD binds to and activates only one type of seotonin receptor.

This is incorrect. LSD, like most ergolines, tends to be extremely non-selective. LSD binds to 5ht2a, 5ht2c, 5ht1a, 5ht1e, 5ht5a, 5ht6, and 5ht7 receptors, with strong affinities for everything except for 5ht1e. It also activates most DAergic & NEergic receptors, with various agonist and antagonist effects.

5ht2a activity mediates its classic psychedelic effects, but various psychedelic phenethylamine/amphetamine derivatives tend to be much more selective for it.

Do you mean the difference between dopamine and serotonin? It's difficult to boil it down to a distinct difference because, as Doofangoodle said, they both have a variety of different actions depending on what area of the body/brain you're looking at. If you look at the disorders from low and high levels of each you get a general idea; low dopamine levels contribute to development of Parkinson's disease (rigid muscle movement, cognitive impairments, memory loss). Too much dopamine is found in conditions such as schizophrenia (hallucinations, muscle spasms). Low serotonin, again like Doofangoodle said is implicated in depression (low mood, increased inhibitions, lethargy), while too much serotonin (usually from overmedication) leads to nausea, confusion and flu-like symptoms.

Regarding dopamine: Elevated levels can lead to schizophrenic behavior (this is theoretical and probably over simplified...). Antipsychotic drugs work on blocking dopamine receptors.

Decreased levels lead to Parkinson disease (it is really a decrease in receptors but you get the point). Patients with Parkinson's disease are given dopamine (again simplified) and other drugs that help elevate dopamine.

I'm sure you know what you meant, but just to correct that for the sake of anyone else reading it, the symptoms of Parkinson's is caused by the death of Dopamine producing neurons in a tiny part of the brain called the substantia nigra. When these neurons die off, less dopamine is able to be released into the motor control loop of the basal ganglia making movement more difficult.

The brain is pretty much a giant interconnected machine that is heavily compartmentalized. Everything talks to each other, and this is done primarily through neurotransmitters. Neurotransmitters act on other neurons to activate, inhibit, or generally cause a downstream signaling cascade that leads to some sort of change. They do this through binding to proteins called receptors and transporters found on the neurons they are acting on which are specific for them.

It's not really the best idea to try and lump neurotransmitters with specific tasks or outputs. The only time it's fair to do that is with the almost always inhibitory neurotransmitter, GABA, and the excitatory neurotransmitter, glutamate. GABA and glutamate neurons release their neurotransmitters and cause inhibition and excitation, respectively, on whatever neurons they are synapsing with.

For an example of the complexity, let's look at dopamine. This neurotransmitter is crucial to movement, reward, arousal, and a whole lot of other cognitive functions (but again not SOLELY involved). If we look specifically at its role in movement (as part of what's known the basal ganglia circuit) [here] (http://journals.cambridge.org/fulltext_content/ERM/ERM5_10/S1462399403006008sup004.htm), you can see dopamine released from the SNc causes activation or inhibition of widespread glutamatergic or GABAergic pathways that ultimately lead to movement.

Unlike glutamate and GABA, which usually stay true to their roles, the role of dopamine is heavily governed by whatever receptor is present on what they are released onto. Dopamine, for example, has 2 families of receptors that can lead to inhibitory or excitatory actions. So dopamine released one place can stop a whole circuit, or it can activate it in another.

This is just one of an untold number of circuits that the brain has and should give you a clue as to why drugs that act on these basic systems can have so many widespread side-effects throughout the brain.

The functions of various neurotransmitters actually depend on the receptor of the neurotransmitter. For example, oxytocin can both stimulate the cervix and uterus during labor to facilitate the birthing process, and it can also stimulate the release of milk from the mammary glands in a new mother.

It helps to differentiate two things: neurotransmitters, and neuromodulators. The first category are used for transmitting information, since they are very temporally and spatially precise and they can reliably transfer information. On the other hand, the second category is used for modulation of neural activity; they are not as temporally or spatially precise as the first category. The chemicals that you mentioned belong to the second category. Here is an example, if you are looking at a light, you need neurotransmitters to reliably transfer that information in the brain (such as Glutamate and GABA). But if it turns out that this light is a salient stimulus, for example, it means danger, then you need neuromodulators to be released and "highlight" the importance of information that is transmitted by neurotransmiters, i.e. stamp it with an emotional gloss in different parts of brain. Neuromodulators by themselves usually don't evoke a major response in brain, but they change the brain response to neurotransmitters. They are important for learning, attention etc. depending on which neuromodulator you are talking about.